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Background  The white-rot fungi in the genus  Ganoderma  interact with both living and dead angiosperm tree hosts. Two  Ganoderma  species, a North American taxon,  G. zonatum  and an Asian taxon,  G. boninense , have primarily been found associated with live palm hosts. During the host plant colonization process, a massive transcriptional reorganization helps the fungus evade the host immune response and utilize plant cell wall polysaccharides.    Results  A publicly available transcriptome of  G. boninense  - oil palm interaction was surveyed to profile transcripts that were differentially expressed  in planta . Ten percent of the  G. boninense  transcript loci had altered expression as it colonized oil palm plants one-month post inoculation. Carbohydrate active enzymes (CAZymes), particularly those with a role in lignin degradation, and auxiliary enzymes that facilitate lignin modification, like cytochrome P450s and haloacid dehalogenases, were up-regulated  in planta . Several lineage specific proteins and secreted proteins that lack known functional domains were also up-regulated  in planta , but their role in the interaction could not be established. A slowdown in  G. boninense  respiration during the interaction can be inferred from the down-regulation of proteins involved in electron transport chain and mitochondrial biogenesis. Additionally, pathogenicity related genes and chitin degradation machinery were down-regulated during the interaction indicating  G. boninense  may be evading detection by the host immune system.    Conclusions  This analysis offers an overview of the dynamic processes at play in  G. boninense  - oil palm interaction and provides a framework to investigate biology of  Ganoderma  fungi across plantations and landscape.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12864-021-07644-9.

bmc genomics

Transcriptional profile of oil palm pathogen, Ganoderma boninense, reveals activation of lignin degradation machinery and possible evasion of host immune response